ArticleCellular immunology2013
Hypoxia and cytoplasmic alkalinization upregulate growth hormone expression in lymphocytes.
Article in Cellular immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Gestation Regulates Growth Hormone and Its Receptor Expression in Sheep Immune Organs.Biology · 2025Article
- C4orf47 contributes to the dormancy of pancreatic cancer under hypoxic conditions.Journal of Cancer · 2023Article
- Optical Control of CD8Frontiers in immunology · 2021Article
- Effects of somatotropic axis on cognitive dysfunction of obstructive sleep apnea.Sleep & breathing = Schlaf & Atmung · 2020Article
- Significance of preoperative total lymphocyte count as a prognostic criterion in adult cardiac surgery.Anesthesiology and pain medicine · 2014Article
- Expression of lymphocyte-derived growth hormone (GH) and GH-releasing hormone receptors in aging rats.Cellular immunology · 2013Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
We report here that culture of lymphoid cells under hypoxic conditions showed an increase in both luciferase expression from a GH-promoter luciferase construct and the levels of lymphocyte GH. The effect was mimicked by treatment of cells with cobalt chloride consistent with a specific oxygen-sensing mechanism. We identified a putative hypoxia response element (HRE) in the GH promoter at the region -176 bp to -172 bp that contains a copy of the hypoxia-inducible factor-1 (Hif-1) binding motif (5'-ACGTG-3'). The results also showed that culture of primary rat spleen cells with different doses of TMA induced a dose-dependent increase in lymphocyte GH by Western blot analysis. Greater levels of GH are induced in T cell-enriched populations compared to B cell-enriched populations after treatment with CoCl(2) or TMA. Our results suggest that the stressful cellular conditions likely to occur at sites of inflammation or tumor growth may induce the synthesis of lymphocyte GH.
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Registered trials
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